GLP-1 receptor agonist: difference between revisions
Diff·revision 7 → 8·02:39, 14 Aug 2024
Difference between revision 7 and revision 8 of GLP-1 receptor agonist. 7 lines changed; the page grew by 740 bytes.
| Revision 7 — 13:36, 31 Jul 2024 StubSorterBot (talk) bot: sort category members 4,181 bytes +1,393 | Revision 8 — 02:39, 14 Aug 2024 FigureFerdinand (talk) give the isoelectric point with the method it was determined by 4,921 bytes +740 | ||
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| 4 | | Molecular target = [[GLP-1 receptor]] (GLP1R) | 4 | | Molecular target = [[GLP-1 receptor]] (GLP1R) |
| 5 | | First approval = Exenatide, 2005 | 5 | | First approval = Exenatide, 2005 |
| + | 6 | <!-- Members in clinical use --> | |
| + | 7 | | Peptide, daily = [[Liraglutide]], [[Exenatide]], [[Lixisenatide]] | |
| + | 8 | | Peptide, weekly = [[Semaglutide]], [[Dulaglutide]] | |
| + | 9 | | Oral peptide = [[Oral semaglutide]] | |
| + | 10 | | Small molecule = [[Orforglipron]] (investigational) | |
| 6 | }} | 11 | }} |
| 7 | 12 | ||
| ⋮ | ⋮ | ||
| 16 | 21 | ||
| 17 | At the beta cell, the rise in cAMP amplifies glucose-stimulated [[Insulin secretion|insulin secretion]] without initiating it. Because the amplification requires a permissive glucose signal, agonism does not provoke insulin release at low glucose, and monotherapy carries a low intrinsic risk of [[Hypoglycaemia|hypoglycaemia]] — a property that distinguishes the class sharply from sulfonylureas.{{r|nauck2016}} | 22 | At the beta cell, the rise in cAMP amplifies glucose-stimulated [[Insulin secretion|insulin secretion]] without initiating it. Because the amplification requires a permissive glucose signal, agonism does not provoke insulin release at low glucose, and monotherapy carries a low intrinsic risk of [[Hypoglycaemia|hypoglycaemia]] — a property that distinguishes the class sharply from sulfonylureas.{{r|nauck2016}} |
| + | 23 | ||
| + | 24 | Three further actions contribute to the clinical effect. Glucagon secretion from alpha cells is suppressed in a similarly glucose-dependent manner, reducing hepatic glucose output. [[Gastric emptying|Gastric emptying]] is delayed, blunting the postprandial glucose excursion and contributing to early satiety. Central agonism reduces food intake, and this — rather than any effect on energy expenditure — accounts for the great majority of weight loss observed in trials.{{r|drucker2018}} | |
| 18 | 25 | ||
| 19 | == Molecular strategies for half-life extension == | 26 | == Molecular strategies for half-life extension == |